ArticleCell death and differentiation2025
Dynamic 3D genome reorganization during senescence: defining cell states through chromatin.
Article in Cell death and differentiation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
36 citing papers in PubMed, 47 citations in OpenAlex.
- The responsive nucleus: morphological signatures of cellular state.Nucleus (Austin, Tex.) · 2026Review
- Reversing aging-like 3D genome disorganization in abioRxiv : the preprint server for biology · 2026Article
- Systemic epigenetic dysregulation as a driver of ageing and a therapeutic target.Nature reviews. Molecular cell biology · 2026Review
- Therapy-induced senescent cancer cells as bidirectional regulators of antitumor immunity and resistance in the tumor microenvironment.Cell death & disease · 2026Review
- Replicative senescence induction in single cells is not predicted by telomere length, dysfunction, or oxidation.iScience · 2026Article
- Hypoxia Preserves Chromatin Integrity and Delays Cellular Senescence through Epigenetic Regulation.Biomolecules & therapeutics · 2026Review
- Natural Products as Anti-Senescence-Associated Secretory Phenotype (SASP) Agents.Current medicinal chemistry · 2026Review
- Cellular Senescence as a Risk Factor in Head and Neck Cancer-Diagnostic and Therapeutic Perspective.Cancers · 2025Review
- The Nutrigenomic Effect of Mela Rosa Marchigiana Callus Extract on Cellular Senescence: Insight From a Preliminary In Vitro Study.Molecular nutrition & food research · 2025Article
- Super-Resolution Compatible DNA Labeling Technique Reveals Chromatin Mobility and Organization Changes During Differentiation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Identifying regulators of aged fibroblast activation in 3D tissue models.Scientific reports · 2025Article
- Biomolecular Fingerprints of Sirtuin Activity in Senescent Fibroblasts Identified via Synchrotron-Based FTIR.International journal of molecular sciences · 2025Article
- Article
- Interrogating the regulatory epigenome of cellular senescence.Cellular and molecular life sciences : CMLS · 2025Review
- The states of senescent cells.Biochemical Society transactions · 2025Review
- Early-stage administration of hydroxytyrosol extends lifespan and delays aging in C. elegans.Biology direct · 2025Article
- Emerging roles for the nucleolus in development and stem cells.Development (Cambridge, England) · 2025Review
- Tracing Cellular Senescence in Bone: Time-Dependent Changes in Osteocyte Cytoskeleton Mechanics and Morphology.Small (Weinheim an der Bergstrasse, Germany) · 2025Article
- Integrative analysis of gene expression and chromatin dynamics multi-omics data in mouse models of bleomycin-induced lung fibrosis.Epigenetics & chromatin · 2025Article
- UV-induced reorganization of 3D genome mediates DNA damage response.Nature communications · 2025Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cellular senescence, a cell state characterized by growth arrest and insensitivity to growth stimulatory hormones, is accompanied by a massive change in chromatin organization. Senescence can be induced by a range of physiological signals and pathological stresses and was originally thought to be an irreversible state, implicated in normal development, wound healing, tumor suppression and aging. Recently cellular senescence was shown to be reversible in some cases, with exit being triggered by the modulation of the cell's transcriptional program by the four Yamanaka factors, the suppression of p53 or H3K9me3, PDK1, and/or depletion of AP-1. Coincident with senescence reversal are changes in chromatin organization, most notably the loss of senescence-associated heterochromatin foci (SAHF) found in oncogene-induced senescence. In addition to fixed-cell imaging, chromatin conformation capture and multi-omics have been used to examine chromatin reorganization at different spatial resolutions during senescence. They identify determinants of SAHF formation and other key features that differentiate distinct types of senescence. Not surprisingly, multiple factors, including the time of induction, the type of stress experienced, and the type of cell involved, influence the global reorganization of chromatin in senescence. Here we discuss how changes in the three-dimensional organization of the genome contribute to the regulation of transcription at different stages of senescence. In particular, the distinct contributions of heterochromatin- and lamina-mediated interactions, changes in gene expression, and other cellular control mechanisms are discussed. We propose that high-resolution temporal and spatial analyses of the chromatin landscape during senescence will identify early markers of the different senescence states to help guide clinical diagnosis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.